1. Field of the Invention
The present invention relates to catechin-related compositions to lower postprandial blood glucose elevation. The present invention also relates to functional foods for blood glucose control containing green tea extracts (GTE) with gallated catechins (GC) and macromolecules that prevent intestinal absorption of GC. One purpose of this invention is to take blood glucose lowering compositions after a meal without any side effects by inhibiting intestinal glucose absorption as well as lipid absorption using a different mechanism from available hypoglycemic agents.
2. Description of the Related Art
Type 2 diabetes is characterized by two main features: peripheral insulin resistance and beta-cell dysfunction. Both hereditary and environmental factors, such as obesity and prolonged hyperglycemia, may trigger or exaggerate human type 2 diabetes. Hyperglycemia causes both beta-cell damage and peripheral insulin resistance via multiple mechanisms, collectively referred to as glucotoxicity (Borona, 2008). In MODY-2 diabetes, functional defects in glucokinase genes restrict hepatic glucose uptake, bringing about prolongation of postprandial hyperglycemia (Jiang et al., 2008), and eventually result in beta-cell overload. Hence, efforts to minimize postprandial hyperglycemia, as well as fasting blood glucose control, are of importance for the prevention and treatment of type 2 diabetes. Although amylase inhibitors or glucosidase inhibitors are available to date to decrease postprandial hyperglycemia, the usage can induce some gastrointestinal side effects, as they block the conversion to monosaccharide. The leaves of green tea (Camellia sinensis) contain polyphenols, in which catechin family is the most major polyphenol. Catechins extracted with water from green tea leaves contain gallated catechins (GC), which mainly include gallate, epicatechin gallate (ECG) and epigallocatechin gallate (EGCG). With regard to type 2 diabetes, the effects of green tea extracts (GTE) or EGCG in in vitro and in vivo studies were intensively investigated. However, the debate over whether GTE or EGCG is actually applicable for the prevention or treatment of human obesity and type 2 diabetes has not been settled (Anderson & Polansky, 2002; Fukino et al., 2005; Naftalin et al., 2003). Daily consumption of green tea by diabetic humans over a period of several months was recently revealed to be ineffective in alleviating blood glucose levels, HbA1C levels, insulin resistance and inflammation markers (Fukino et al., 2005). Interestingly, it has been demonstrated that orally-applied GTE may inhibit glucose (Johnston et al., 2005; Kobayashi et al., 2000; Zhu et al., 2001) and cholesterol (Raederstorff et al., 2003) absorption from the alimentary tract. This is thought to be one of the underlying mechanisms by which GTE influences type 2 diabetes and obesity. Gallated catechins (GC), including EGCG and epicatechin-3-gallate (ECG), appear to be responsible for the inhibitory effects, mainly through the inhibition of Na-glucose co-transporters (SGLT1) in the intestinal epithelia (Kobayashi et al., 2000) and mixed micelle formation in the intestinal lumen (Raederstorff et al., 2003). The amount of GC that needs to be ingested to exert the luminal effect appears to be endurable in humans (Kobayashi et al., 2000; Van Amelsvoort et al., 2001), probably due to the lower oral bioavailability of these molecules. Nevertheless, a certain proportion of the ingested catechins is inevitably absorbed into the blood and acts at other sites within the body. Therefore, the effects of orally-ingested GTE on glucose and lipid metabolism are the combination of the effects in the alimentary tract and in the circulation. Some reports demonstrated that oral application of GTE in rats (Sabu et al., 2002) and humans (Tsuneki et al., 2004) decreased blood glucose levels during an oral glucose tolerance test (OGTT). However, these results could be attributed to the luminal effect of GC (Naftalin et al., 2003) because the high glucose was applied immediately after the catechin ingestion. In addition, as rats have very low oral bioavailability of GTE, during the experiment, it is more difficult to detect the effect of GTE after GTE is absorbed in the circulation. This prompted us to evaluate the effects of GTE and EGCG in the circulation as well as in the alimentary tract.
The inventor discovered that GC in the circulation increased blood glucose levels and thus induced insulin hypersecretion. Therefore, a combinatorial application of GTE with an inhibitor of intestinal GTE absorption could effectively obtain the positive GTE effect in the intestinal lumen to lower postprandial blood glucose elevation.